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Contrary to what we wrote, there is clinical evidence that Zocor (unlike Zetia) can reduce the risk of heart attacks and other adverse cardiac events. We relied on a statement in USA Today, and should have checked its accuracy.

That said, let's move on to the subject of today's article about cholesterol.

Cholesterol is an essential component of many key body structures and functions, and driving levels too low can lead to depression, anxiety, and other problems.

Cholesterol: The essential, inaccurately demonized compound

Cholesterol is manufactured in the liver, and many people do not realize that this waxy substance is essential for a wide range of normal body functions, or that dietary cholesterol has little influence on levels of cholesterol in the blood or the risk of developing cardiovascular disease (CVD).

(Given the wide variations in human physiology, one wonders whether the risks of lowierng cholesterol to this rock-bottom level outweigh the cardiac rewards.)

The body regulates cholesterol levels in response to its own complex, little-understood needs. In this context, cholesterol-lowering drugs constitute blunt instruments against CVD: tools that may have unknown long-term impacts.

These are the roles that cholesterol is known to play in the body, with others no doubt remaining to be discovered:

Cholesterol is an essential component of all cell membranes, where it regulates their fluidity, preventing them from becoming both too rigid or fluid.

Cholesterol is a primary component of cellular “lipid rafts,” and in this role, it facilitates a key bodily process called “cell signaling”. Among other functions, cholesterol-mediated cell-signaling enables neurons (brain cells) to find each other when forming synapses critical to learning and memory.

Cholesterol helps guide the connecting parts of neurons to the right places, and is necessary for their ability to grow.

High cholesterol levels are associated with increased risk of heart attacks and other adverse heart events, and the clinical evidence shows that some cholesterol-lowering statin-type drugs reduce heart attacks and deaths.

However, the hypothesis that high cholesterol levels cause cardiovascular disease and related deaths is increasingly questioned. As the author of one evidence review wrote, “The evidence establishes that the lipid hypothesis of atherosclerosis lacks scientific basis” (Stehbens WE 2001).

In fact, some population groups with high cholesterol levels and high intakes of saturated fat—such as the French—enjoy low rates of heart disease.

It looks more and more like the anti-inflammatory effects of statins may be the main source of their cardiac benefits, rather than their ability to lower cholesterol.

The team recruited 55 men and women, ages 60-69, who were healthy non-smokers and were able to perform exercise testing and training.

For three months, participants performed several exercises, including stretching, stationary bike riding and vigorous weight lifting, three days a week.

All the volunteers consumed similar diets.

At the end of the 12-week study, those with higher cholesterol intake or higher blood levels of cholesterol and those taking statin drugs had the greatest muscle strength gains.

(Higher intake of protein did not yield greater gains in muscle mass.)

The scientists noted that cholesterol facilitates the body’s inflammatory immune response to the damage that exercise does to muscle, and that this inflammation response stimulates the body’s muscle-building “anabolic” processes.

(While chronic inflammation in arteries or other tissues is unhealthful, short-lived inflammation is an integral part of the muscle-building process.)

In addition, they observed that cholesterol probably serves as an essential building block for repair of the “micro-tears” that occur in muscle membranes stressed by exercise.

And, as noted previously, cholesterol is essential to the formation of lipid rafts. These cellular structures facilitate growth of muscle in response to resistance exercise training such as weight lifting.

Surprisingly, statins seemed to aid strength gains as well

The research team was surprised to find greater strength gains among the participants taking cholesterol-lowering statin drugs.

This was unexpected, considering three factors:

Statins lower blood cholesterol levels.

Statin drugs are generally anti-inflammatory.

Some statins are associated with a minor risk of muscle pain and weakness.

However, statins increase the susceptibility of muscle to injury in response to exercise, which in turn may stimulate production of inflammation-related growth factors that promote muscle growth.

In addition, statins influence production of compounds (isopentenyl-pyrophosphate and selenoproteins) in ways that may explain the unexpected increase in muscle strength among the statin-users in the study.

The authors noted that results of this trial conflict with recommendations to lower cholesterol levels in order to prevent cardiovascular disease (CVD).

As they wrote, “The evidence that higher serum [blood] cholesterol is associated with greater risk for CVD is clear… Because [elevated] cholesterol… [raises the risk of CVD] rigorous efforts to confirm these findings are necessary. Even if results are confirmed, it is necessary to examine changes in cardiovascular risk due to dietary cholesterol consumption (within the context of exercise training) so that reduction in sarcopenia [muscle weakness] and disability is not at the price of elevated CVD” (Riechman SE et al. 2007).

And they noted that the study participants with higher cholesterol levels were more likely to have higher levels of an inflammatory chemical and CVD risk factor called CRP.

The researchers were refreshingly honest in the conclusion to their press release: “…there is still a lot about cholesterol that we don’t know” (Texas A&M University 2008).